Immune thrombocytopenic purpura (ITP) is characterized by autoantibody-mediated thrombocytopenia,with the major autoantigens being platelet glycoproteins.Cellular immunity is also involved in platelet destruction.ITP remains a diagnosis of exclusion,defined as primary and secondary ITP.The major goal for its treatment is to provide a safe platelet count.Corticosteroid-based regimens are commonly used as the initial treatment,and severe patients have temporary responses to intravenous immunoglobulin.Splenenectomy shows curative-potential in some chronic ITP cases.Thrombopoietic agents would become a new approach of treatment.Helicobacter pylori (H.pylori) infection should be screened in adult chronic ITP,and when the result is positive,H.pylori eradication therapy is indicated.

SJAMP and HLAMP are glucose-containing acidic mucopolysacc-harides isolated from sea cucumbers, Stichopus Japonicus and Holot-huria Lecospilota respectively. Their effects on the interaction of thrombin with endothelial cells were studied. Human vascular endothelial cells isolated from umbilical veins treated with 0.1% collagenasc were cultured with MEM medium. The contents of von Willebrand factor (vWF) and 6-keto-PGFla, stable hydrolysis product of PGI,, in the culture medium were measured with ELISA and immunoradioassay technique. The addition of thrombin to confluent monolayer endothelial cells resulted in a significant increase in the release of vWF and 6 ~ keto-PGFla in the culture medium. When heparin,SJAMP or HLAMP was added, no significant amount of vWF or 6~keto-PGFla could be detected in the medium .Whereas preincubation of thrombin with heparin, SJAMP or HLAMP respectively inhibited the thrombin-induced vWF and 6-keto-PGF 10 release and this effect was well correlated with the dose of heparin, SJAMP or HLAMP, indicating that SJAMP, HLAMP as well as heparin had inhibitory effect on the interaction of thrombin with endothelial cells

Objective To measure von Willebrand factor(vWF)concentrations and von Willebrand factor-cleaving protease(vWF-cp)activity in plasma of lung cancer patients and to evaluate their clinical significance.Methods The vWF:antigen(vWF:Ag)and vWF-cp activity were measured by using ELISA and residual-collagen binding assay(R-CBA),respectively in 78 patients with lung cancer.The serum and pleural fluid(PLF)of carcino-embryonic antigen(CEA)were measured by radioimmunity assay in 23 patients.Results (1)The level of vWF:Ag in lung cancer patients(107.7?43.7)%was significantly higher than that in benign diseases(71.3?49.5)% and normal controls(82.4?41.3)%(P

Quercetin (0.05~0.20 mmol/L, final concentration) obviously inhibited the aggregation and production of PGE2 and TXB2 of human PMN which were induced by AA ( 0.66 mmol/L), LTB4 ( 0.002 mmol/L) and the fourth composition of cobra venom of Guangxi Province ( 4.8mg/L) in vitro. These effects were dose dependent, the IDg50 of PMN aggregation induced by AA, LTB4 and the fourth composition of cobra venom of Guangxi Province was 68?mol/L, 59?mol/L and 61?mol/L respectively. At the concentration of 0.50?mol/L, it can also inhibit lysozyme release of PMN induced by AA, LTB4 and the fourth composition of cobra venom of Guangxi Province.

Objective To compare the level of Annexin Ⅱ in patients with systemic lupus erythematosus(SLE),diabetic nephropathy(DN),chronic glomerulonephritis and normal controls,and explorle the significance of the annexin Ⅱ in SLE.Methods Thirty-five cases of patients with SLE,ten cases of patients with DN,ten cases of patients with chronic glomerulonephritis were enrolled in this study,twenty cases of healthy controls were also enrolled.Circulating annexin Ⅱ in white blood cells was detected bv flow cytometry.Student's t test,variance analysis and Lineat correlation analysis were used for statistial analysis.Resuits Compared with healthy controls,the level of annexin Ⅱ in white blood cells in SLE patients (7.1±2.9)%and DN patients(8.0±3.7)%were significantly lower than that of the healthy controls(P<0.01,p<0.05).In the SLE group,the level of annexin Ⅱ of patients who had more active disease(SLEDAI≥9)decreased more thall those with less active disease(SLEDAI<9),(P<0.05).A positive correlation was found between annexin Ⅱ and serum albumin level(r:0.439,P<0.01),but negative correlation was found between annexin and urine protein/urine creatinine(r=-0.382,P<0.05),SLEDAI(r=-0.417,P<0.05),D-dimer(r=-0.336.p＜0.05) levels.Conclusion The level of annexin Ⅱ is decreased in patients with SLE,so it can renectthe abnormality of coagulation and fibrinolytic systems,and it may be used as a good indicator for prothrombotic status in SLE patients.It can be helpful to evaluatethe activity of the disease and the therapeutic efficacy.

Objective To explore the gene sequencing and prenatal diagnosis of Glanzmann thrombasthenia (GT). Methods The blood samples were drawn from one case of phenotype GT pediatric patient, patient’s parents, and one normal control. The amniotic lfuid and cord blood from the fetus of patient’s mother were collected. When the fetus was born 2 days, the blood was drawn. The coagulation routine test and platelet aggregation test were performed. The expression of platelet membrane glycoprotein (GP) IIb and GPIIIa were tested by lfow cytometry. Microsatellite technology is used to determine whether fetal cord blood is contaminated with maternal cells. The expressed region and the junctional zone between exon and introns of GPIIb and GPIIIa were ampliifed by PCR technology from blood sample of patient, patient’s parents, and fetus’s cord and 2 days after birth. The PCR products were then subjected to DNA sequencing. Results Adenosine diphosphate (ADP) cannot induce the platelet aggregation in the patient. The max rate of the platelet aggregation in the fetus’s cord blood was half of the normal. However, the max aggregation rate induced by ADP in the blood sample of parents and fetus 2 days after birth were equal to normal. The mean lfuorescence intensity (MnX) of platelet membrane GPIIb and GPIIIa in the patient were 10%and nearly zero of the normal control, respectively, while those in the parents, the fetus’s cord blood and 2 days after birth were more than 90%and 30%to 50%of the normal control. The cast-off cells in amniotic lfuid and the DNA in cord blood analysis by microsatellite technology conifrmed that the amniotic lfuid and cord blood not contaminated by maternal cells. Gene analysis showed the heterozygosis mutation in exon6 A3829→C and exon9 G42186→A of the patient’s GPIIIa led to the amino acid heterozygosis mutation in GPIIIaHis281→Tyr and Cys400→Pro. These two mutations came from the father and the mother separately. However, there was only one heterozygosis mutation in exon9 G42186→A in the cast-off cells in amniotic lfuid, the fetus’s cord and blood 2 days after birth. Conclusion This GT patient have double heterozygosis mutation. The fetus has heterozygosis mutation conifrmed after birth.

AIM:To study the relation between expression of uPAR and annexinⅡ and fibrinolytic activity in various leukemic cell lines.METHODS: The plasma activity was measured under the reaction between cells of NB4,SHI-1,K562,Jurkat,Raji and plaminogen by chromogenic assay.The protein expressions of uPAR and annexinⅡin cells of NB4,SHI-1,K562,Jurkat,Raji were detected by flow cytometry method.The mRNA expressions of uPAR and annexinⅡin cells of NB4,SHI-1,K562,Jurkat,Raji were detected by RT-PCR.RESULTS: The plasma activity in SHI-1 cells and NB4 cells were higher obviously than that in Raji,K562 and Jurkat cells.The protein expression ratio of uPAR and annexinⅡ in NB4 cells were(13.15?1.61)% and(95.97?1.19)%,respectively,they were(99.00?0.26)%,(90.35?2.15)% respectively in SHI-1 cells,and they were lower in K562,Jurkat,Raji cells.The expression of annexinⅡ mRNA in NB4 cells was higher than that in SHI-1 cells,and they were undectectable in K562 and Jurkat cells.The expression of uPAR mRNA in NB4 and SHI-1 cells were higher than that in Jurkat and K562 cells.The expression of uPAR mRNA in Raji cells was undectectable.CONCLUSION: The primary hyperfibrinolysis in leucocythemia cells was observed,and relation was closely with the expression of annexinⅡ.It might be the main reason for bleeding and disseminated intravascular coagulation in patients with acute promyelocytic leukemia and acute monocytic leukemia.

Objective To explore the diagnostic value of protein induced by vitamin K absence or antagonist-Ⅱ (PIVKA-Ⅱ) in non-infant with acquired deficiency of vitamin K-dependent coagulation factors (ADVKCF).Methods PIVKA-Ⅱ levels were measured by ELISA in 50 patients with ADVKCF on day 0,3,7 after vitamin K treatment.Prothrombin time(PT),APTT,FⅡ ∶ C,FⅦ∶ C,FⅨ∶ C,and FⅩ∶ C were analyzed simultaneously.Twenty healthy subjects were enrolled as controls.Results The average level of PIVKA-Ⅱ in ADVKCF group was (3.83 ± 1.40) μg/L,while (1.30 ± 0.54) μg/L in the control group (P ＜ 0.05).The PIVKA-Ⅱ levels on day 0 and 3 did not show significant difference [(3.83 ± 1.40) μg/Lvs (3.79 ± 0.66) μg/L,P ＞ 0.05],but decreasing significantly on day 7 compared to the control group (P ＜ 0.05).The PIVKA-Ⅱ level was (3.78 ± 1.30) μg/L in patients receiving plasma transfusion,while (3.91 ± 1.49)μg/L in no-plasma-transfusion group (P ＞ 0.05).Coagulation factors Ⅱ,Ⅶ,Ⅸ and Ⅹ activity which decreased significantly before treatment returned to normal range after one week use of vitamin K,leading to complete correction of prolonged APTT and PT (＞ 100 seconds).Conclusions The PIVKAⅡ level in ADVKCF patients is significantly higher than that of healthy subjects within one week treatment of vitamin K,which is not influenced by plasma transfusion.This study suggests that PIVKA-Ⅱ is a more sensitive parameter than APTT,PT and the activity of coagulation factor,which could be a valuable factor in the early diagnosis of ADVKCF.

Objective To investigate the pathogenesis of renal lesion in Fechtner syndrome . Methods Pathological characteristics of kidney tissues from Fechtner syndrome patients were explored by HE staining, immunochemistry, immunofluorescence and electron microscopy . Results Immunochemistry analysis showed that non-muscle myosin heavy chain IIA (NMMHC-IIA)was expressed in podocytes of giomeruli and distal convoluted tube, and was faintly expressed in the brush border of proximal tube . Histological examination demonstrated glomerulosclerosis and decreased expression of NMMHC-IIA in abnormal podocytes . Through standard immunofluorecence, the expression of NMMHC-IIA in patient's podocyte was higher than that in normal pedocytes . The fusion of foot process and microvillus were detected by electron microscopy . Conclusion Abnormal NMMHC-IIA aggregates in the glomeruli podocyts and foot process fusion accompanied with appearance of microvillus leads to renal lesion in Fechtuer syndrome .

Hepatitis, Viral, Human ; complications ; Humans ; Thrombocytopenia ; etiology ; therapy